Submitted on January 4, 2005
Accepted on July 25, 2005
Autonomic Cardiovascular Regulation in Subjects with Acute Mountain Sickness
Paola A Lanfranchi1*, Roberto Colombo2, George Cremona3, Paolo Baderna4, Liliana Spagnolatti4, Giorgio Mazzuero5, Peter Wagner6, Liliana Perini5, Harrieth Wagner6, Carmelo Cavallaro7, and Pantaleo Giannuzzi5
1 Cardiology, Salvatore Maugeri Foundation, Veruno, Novara, Italy; Centre de Recherche, Hopital du Sacre-Coeur, Montreal, Quebec, Canada
2 Service of Bioengineering, Salvatore Maugeri Foundation, Veruno, Novara, Italy
3 Division of Respiratory Medicine, Salvatore Maugeri Foundation, Veruno, Novara, Italy
4 Department of Radiology, Salvatore Maugeri Foundation, Veruno, Novara, Italy
5 Centre de Recherche, Hopital du Sacre-Coeur, Montreal, Quebec, Canada
6 Unit of Respiratory Medicine, San Raffaele University Hospital, Milan, Milan, Italy
7 Division of Physiology, University of California, San Diego, California, USA
* To whom correspondence should be addressed. E-mail: paola-lanfranchi{at}crhsc.umontreal.ca.
Aims- The aims of the study were: 1)to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction, 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS.
Methods and results. Forty-one mountaineers were studied at 4559 m altitude. AMS was diagnosed using the Lake Louise score, and the autonomic cardiovascular function was explored using spectral analysis of RR interval and blood pressure (BP) variability on 10-minute resting recordings. Seventeen subjects (41%) had AMS. AMS subjects were older than those without AMS (p<0.01). At high altitude AMS subjects had higher low frequency component of systolic BP variability (LFSBP) (p=0.02) and lower LF component of RR variability (LFRRNU) (p=0.001). After 3 months, 21 subjects (43% with AMS), repeated the evaluation at low altitude at rest and in response to hypoxic gas mixture. LFRR NU was similar in the two groups at baseline and during hypoxia at low altitude, but at high altitude increased only in subjects without AMS (p<0.001) and did not change between low an high altitude in AMS subjects. Conversely, LFSBP increased significantly during short-term hypoxia only in AMS subjects, who also had higher resting BP (p<0.05) than those without AMS.
Conclusions- Autonomic cardiovascular dysfunction accompanies AMS. Marked LFSBP response to short term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasocostrictory response to hypoxia in the genesis of AMS.
